ArticlePLoS pathogens2023
Distinct disease features of acute and persistent genotype 3 hepatitis E virus infection in immunocompetent and immunosuppressed Mongolian gerbils.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- p38 Inhibitor SB203580 Inhibits HEV Infection and Prevents HEV-Related Adverse Pregnancy Outcomes in a Pregnant Rabbit Model.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- HEV replication is promoted by blocking the NF-κB signaling pathway through inhibiting FLNa expression.Journal of virology · 2026Article
- Substantial spillover burden of rat hepatitis E virus in humans.Nature communications · 2025Article
- Effect of Hepatitis E Virus on the Male Reproductive System: A Review of Current Evidence.Viruses · 2025Review
- Ancient evolutionary origins of hepatitis E virus in rodents.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Strain- and Subtype-Specific Replication of Genotype 3 Hepatitis E Viruses in Mongolian Gerbils.Viruses · 2024Article
- Hepatitis E virus immunosuppressed animal models.BMC infectious diseases · 2024Review
- Optimization of immunosuppression strategies for the establishment of chronic hepatitis E virus infection in rabbits.Journal of virology · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis E virus (HEV) causes self-limited acute hepatitis in immunocompetent individuals and can establish chronic infection in solid organ transplant recipients taking immunosuppressive drugs. A well characterized small animal model is needed to understand HEV pathogenesis. In this study, we established a robust model to study acute and persistent HEV infection using Mongolian gerbils (Meriones unguiculatus) with or without immunosuppression. Gerbils were implanted subcutaneously with continuous release tacrolimus pellet to induce immunosuppression. Gerbils with or without tacrolimus treatment were inoculated with HEV intraperitoneally. Viremia, fecal virus shedding, serum antibody and ALT levels, liver histopathological lesions, hepatocyte apoptosis, and liver macrophage distribution were assessed. Mild to moderate self-limited hepatitis and IgM and IgG antibody responses against HEV ORF2 were observed in immunocompetent gerbils. Levels of HEV-specific IgM responses were higher and lasted longer in immunocompetent gerbils with higher peak viremia. Persistent viremia and fecal virus shedding with either weak, or absent HEV antibody levels were seen in immunosuppressed gerbils. Following HEV infection, serum ALT levels were increased, with lower and delayed peaks observed in immunosuppressed compared to immunocompetent gerbils. In immunocompetent gerbils, foci of apoptotic hepatocytes were detected that were distributed with inflammatory infiltrates containing CD68+ macrophages. However, these foci were absent in immunosuppressed gerbils. The immunosuppressed gerbils showed no inflammation with no increase in CD68+ macrophages despite high virus replication in liver. Our findings suggest adaptive immune responses are necessary for inducing hepatocyte apoptosis, CD68+ macrophage recruitment, and inflammatory cell infiltration in response to HEV infection. Our studies show that Mongolian gerbils provide a promising model to study pathogenesis during acute and persistent HEV infection.
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